Colorectal carcinoma (CRC) is known as the most common cancer. MicroRNAs (miRNAs) have been proven to have important roles in human carcinogenesis by regulating various target genes. Recently, the downregulation of miR-582-5p had been demonstrated in CRC. However, its function and the underlying mechanism in CRC remains unknown. In this study, we found that miR-582-5p was frequently downregulated in CRC tissues compared with corresponding noncancerous tissues, as well as in CRC cell lines. Transfection with miR-582-5p mimics significantly inhibited CRC cell proliferation, invasion and arrested cell cycle at the G1/S phase, but promoted cell apoptosis. Further analysis demonstrated that miR-582-5p attenuated the expression of RAS-related GTP-binding protein (Rab27a). Luciferase reporter assay confirmed that Rab27a was a target of miR-582-5p. Mechanism analyses revealed that Rab27a overexpression significantly attenuated the inhibitory effect of miR-582-5p on CRC cell growth, invasion and cell cycle progression. Our data suggest that miR-582-5p may function as a tumor suppressor in the development of CRC by targeting Rab27a, indicating a novel therapeutic strategy for patients with CRC.

Arsenic has been associated with significant effects on human health. Exposure to inorganic arsenic has been associated with the changes in gene expression. Promoter of CDKN1A antisense DNA damage activated RNA (PANDAR) expression is induced by p53 protein and DNA damage response. Here, we investigated whether the ability of arsenic metabolism in individuals affected the expression of PANDAR, DNA damage, and DNA methylation. Levels of gene expression and DNA damage were examined by the quantitative polymerase chain reaction and DNA methylation was measured by the methylation-sensitive high-resolution melting curve. In our study, we demonstrated that arsenic exposure increased PANDAR expression and DNA damage among arsenic smelting plant laborers. The PANDAR expression and DNA damage were positively linked to monomethylarsonic acid % ( R = 0.25, p < 0.05 and R = 0.32, p < 0.01) and negatively linked to dimethylarsinic acid % ( R = −0.21, p < 0.05 and R = −0.31, p < 0.01). Subjects with low primary methylation index had increased levels of DNA damage (51.62 ± 2.96 vs. 60.93 ± 3.10, p < 0.05) and methylation (17.14 (15.88–18.51) vs. 15.83 (14.82–18.00), p < 0.05). Subjects with low secondary methylation index had increased levels of PANDAR expression (4.88 ± 0.29 vs. 4.07 ± 0.23, p < 0.01) and DNA damage (17.38 (15.88–19.29) vs. 15.83 (14.82–17.26), p < 0.01). DNA methylation of PANDAR gene was linked to the regulation of its expression in peripheral blood lymphocytes among laborers ( Y = −2.08 × X + 5.64, p < 0.05). These findings suggested arsenic metabolism ability and exposure affected the expression of PANDAR, DNA damage, and DNA methylation.